Cartilage changes in osteoarthritis include fibrillation and loss of proteoglycans. It has been hypothesized that fibrillation creates large osmotic pressure gradients which cause disruption of the collagen matrix and loss of proteoglycans. We have recently shown that fine fragmentation of normal articular cartilage increases the extractability of proteoglycans with low ionic strength buffer. We have developed a method to reassociate extracted proteoglycans back into extracted cartilage with or without other extractable cartilage components. With this method, it is possible to put varying concentrations of homogeneous proteoglycans into cartilage slices of specific thickness. The method will be used to study two aspects of proteoglycan entrapment: the functional size of the collagen mesh, and swelling or disruption of collagen mesh at the cartilage surface as a result of exposure to low ionic strength solutions. The functional size of the collagen mesh will be determined by separately reassociating non-aggregating proteoglycans of various sizes into large cartilage slices, with small surface area, then re-extracting with a physiologic buffer. The size of the proteoglycans reassociated will be correlated with their resistance to re-extractions. To determine if decreasing the thickness of cartilage results in loss of the ability of the mesh to restrain the expansive pressure of proteoglycans, changes in volume and water content will be noted after reassociation of proteoglycans into various thicknesses of cartilage. To determine if osmotic pressure gradients cause disruption of the superficial collagen mesh, cartilage of varying thicknesses will be extracted for prolonged periods with low ionic strength buffer. The integrity of the mesh will be assessed by its resistance to thermal shrinkage and its capacity to reassociate proteoglycans. These same techniques will then be applied to the study of osteoarthritic cartilage to document the defect present in fibrillated cartilage and to determine if non-fibrillated osteoarthritic cartilage mesh is predisposed to collagen expansion or disruption.